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Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. The vessel may be any vein or artery as, for example, in a deep vein thrombosis or a coronary (artery) thrombosis. The annual incidence of venous thrombosis, one of the leading causes of mortality and morbidity, increases from 1 per 100,000 during childhood to 1 per 100 in old age.

Endothelium plays important role in hemostasis processes of vessels. Through its ability to express procoagulants and anticoagulants, vasoconstrictors, and vasodilators, as well as key cell adhesion molecules and cytokines, the endothelium has emerged as one of the pivotal regulators of hemostasis. Under normal conditions, endothelial cells sustain a vasodilatory and local fibrinolytic state in which coagulation, platelet adhesion, and activation, as well as inflammation and leukocyte activation, are suppressed. during states of endothelial disturbances, whether physical (eg, vascular trauma) or functional (eg, sepsis), a prothrombotic and proinflammatory state of vasoconstriction is supported by the endothelial surface. Release of platelet activating factor (PAF) and endothelin-1 promotes vasoconstriction,3 whereas production of von Willebrand factor (vWF), tissue factor (TF), plasminogen activator inhibitor (PAI)-1, and Factor V augment thrombosis. Additionally, in response to endothelial injury, endothelial cells are activated, resulting in increased surface expression of certain cell adhesion molecules (such as P-selectin or E-selectin), promoting the adhesion and activation of leukocytes. This event initiates and amplifies inflammation and thrombosis.

Microparticles (MPs) are involved in the thrombotic process and the amplification of thrombosis. MPs are small (less than 1 micrometer, about the size of a bacterium), phospholipid vesicles shed from platelets, leukocytes, and endothelial cells in a calcium dependent fashion. MPs are a normal constituent of blood and can be isolated from plasma by ultracentrifugation. MPs lack DNA and recent evidence suggests they may carry RNA, and they are protein rich. Venous stasis and ischemia results in the upregulation of P-selectin which localizes prothrombotic MPs to the area of stasis and promotes DVT formation. The P-selectin receptor P-Selectin Glycoprotein Ligand 1 (PSGL-1) is expressed on leukocytes and platelets, as well as on their derived MPs. MPs are not only prothrombotic but also appear to inhibit fibrinolysis. PAI-1 is stored in the α-granules of quiescent platelets.

In addition to natural anticoagulants such as protein C and protein S, physiological clot formation is balanced by a constant process of thrombolysis to prevent pathological intravascular thrombosis. The central fibrinolytic enzyme is plasmin, a serine protease generated by the proteolytic cleavage of the proenzyme plasminogen. Its main substrates include fibrin, fibrinogen, and other coagulation factors. Plasmin also interferes with vWF-mediated platelet adhesion by proteolysis of GpIb.